DESCRIPTION (Adapted from the applicant's abstract and specific aims): The nose functions to warm and humidify inhaled air. Few investigations have addressed this important function in healthy subjects, and none have systematically examined this function in patients with inflammatory nasal disease. The application proposes to investigate the interactions between the physiologic response of warming and humidifying inhaled air and allergic rhinitis, an inflammatory condition affecting over 40 million Americans. Inhaling cold (0 degrees C) and dry (<10% RH) air (CDA) in a laboratory provides a controlled model for evaluating the ability of the nose to warm and humidify air. Induction of an allergic reaction appears to augment the clinical response to the inhalation of CDA. It is also shown that continuous inhalation of warm (37 degrees C), moist (>90% RH) air prior to nasal antigen provocation reduces the immediate allergic response. It is hypothesized that these environmental conditions reduce the activity of the glands, nerves, blood vessels and other resident cells in the nose that are responsible for warming and humidifying inspired air. Thus, when stimulated by antigen, they react less vigorously. The nose provides a readily accessible human model to study the effects of allergic inflammation on the air-conditioning capacity of the nose and the influence of the environment on allergic inflammation. The application proposes to use nasal provocation techniques, a nasopharyngeal temperature and humidity sensor and an environmental chamber to test the hypotheses that: a) the induction of allergic inflammation reduces the ability of the nasal mucosa to warm and humidify CDA; b) the nasal response to CDA of individuals with perennial allergic rhinitis exceeds that of normal individuals; c) treatment of perennial rhinitic subjects with intranasal steroids reduces inflammation and improves the air-conditioning capacity of the nose; d) the symptomatic treatment of CDA induced rhinitis by anticholenergics reduces the ability of the nose to warm and humidify air; e) preconditioning the nasal mucosa in humid environments before antigenic provocation decreases the early, late, cellular and priming responses; and f) exposing the nose to warm, humid environments after antigenic stimulation reduces the subsequent inflammation, whereas exposing the mucosa to a cold, dry environment augments the inflammatory response. These experiments may expand our knowledge of the nasal response to two common environmental conditions and their interactions, potentially leading to new therapeutic strategies.